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INTRODUCTION Submucosal arytenoidectomy is one of many surgical techniques used in the treatment of the median bilateral vocal fold paralysis. The technique evolved from the large extralaryngeal operation to the endoscopic, intralaryngeal procedure. Gradually it excluded tracheostomy from the methods of treatment of dyspnoea caused by bilateral vocal fold paralysis. MATERIALS AND METHODS We present two patients with bilateral vocal fold paralysis with dyspnoea, caused by the neoplastic mass primarily localised in the left lung. In both cases the nonmicrocellular carcinoma was diagnosed. Both patients had the left recurrent laryngeal nerve palsy for more than 18 months and the right nerve palsy for 10-14 days before admission, with concomitant dyspnoea. RESULTS Both patients were successfully extubated, 24 hours after the operation. The breathing improved significantly. None of the patients had to be reintubated or tracheotomized. CONCLUSIONS The Authors conclude, that the arytenoidectomy with laterofixation should be the method of choice in the treatment of the bilateral vocal fold paralysis caused by the lung cancer. The method does not exclude the upper airway from the respiratory tract which is of special importance for the patients with the lung problems.

Cigarette smoking is a major modifiable risk factor for stroke. Smoking dose dependently increases the risk of stroke, especially in patients below 75 years of age. Although smoking cessation is considered as one of the most effective methods of secondary stroke prevention, little is known about nicotine dependence and predictors of smoking cessation after stroke. Identification of such predictors could facilitate the development of anti-smoking interventions in post-stroke patients. Results of previous studies showed that smoking cessation is determined by the interplay of multiple factors, including sociodemographic (gender, age, race, living conditions, employment), clinical (functional status), psychobiological (nicotine dependence, depressed mood) and environmental (smoking household members) factors. Limitations of most studies were relatively small sample sizes and lack of verification of smoking status with a biochemical marker (e.g. expired CO). The aim of this article is to summarize current knowledge about predictors of smoking cessation after stroke.

The problem of diagnosis in the field of head and neck region is still valid. Specific diagnosis and precise estimation of the tumor's size with the use of CT and MRI imaging is generally unsatisfactory. The Positron Emission Tomography (PET) supports this process with additional information about the tumor's metabolism. Numerous publications show that PET-CT has a great influence on the evaluation of the size of the tumor, presence of lymph node metastases, choice of treatment and the prognosis of the recurrence. Cancer cells represent a specific metabolic state. These cells intake large quantities of glucose and utilize it in the process of glycolysis. The oxidative phosphorylation is not efficient in the transformed cells and defects in mitochondrial functions are at the heart of malignant cell transformation. Disruption of the oxidative phosphorylation chain has been described in the neoplasms. As a consequence, in cancer the glycolysis is active even in the normoxic environment. This metabolic shift in cell transformation has been described in early XX century and so called Warburg's hypothesis profoundly influenced the present perception of cancer metabolism, positioning what is termed aerobic glycolysis in the mainstream of clinical oncology. Today we know that neoplastic cells differ at the proteomic level. A subset of different proteins such as hexokinase II or HIF are upregulated. These abnormalities might be used as the neoplastic markers.

Recently published papers report a large number of mitochondrial DNA mutations in many different cancer types, but their significance for electron transport chain proteins remains unknown. This review covers structural mutations of mitochondrial genes, choosing prostate cancer, esophageal cancer and epithelioma as research models. As all mitochondrial genes encode subunits of the electron transport chain, the review focuses on the consequences of structural mutations on cell metabolism.

Endometrial carcinoma is among the most frequently diagnosed gynecological malignancies in highly developed countries. Research has been conducted for 20 years to define the molecular pathology of this disease and much is already known, but adequate prognostic, diagnostic, and monitoring markers are still missing. Recently, mitochondrial research opened a new perspective. The participation of abnormalities of those organelles and mutations of the mitochondrial genome has been defined in some types of cancer and is still under investigation. MtDNA mutations are also found in endometrial adenocarcinoma, although their impact on cell physiology has not been determined so far. Some processes involving mitochondria are widely known and described in numerous papers. These include electron transport and apoptosis, but others await further research. A forward genetics approach has been used in a wide spectrum of projects in which cancer tissue samples were collected from subjects with defined diagnoses and metabolic abnormalities and mtDNA mutations were checked. Thanks to this approach, characteristic patterns of mitochondrial disruption have been assigned to specific types of cancer. This review focuses on the molecular characteristics of endometrial adenocarcinoma with special focus on mitochondrial abnormalities. Research on cancer molecular pathology in endometrial adenocarcinoma may lead to the development of specific screening and/or diagnostic markers.

Data reported until today suggested a pivotal role of nuclear DNA mutations in the process of carcinogenesis. Recently more and more authors claim that disruption of mitochondrial DNA should not be excluded from this analysis. mtDNA have been reported in many cancers of head and neck region. Mitochondrial D-loop has been proven to be mutation hot - spot with majority of mutations in the positions 303 to 315 of poly-C tract. Data show that 37% of patients with premalignant lesions and 62% with carcinoma in situ are positive for mtDNA mutations. Moreover mutations in genes encoding ND2, ND5, COIII, CYTB, and ATP6 were observed in 17% of patients. Mutations in mitochondrial rRNA genes occured in similar number of cases. Neoplastic cells undifferentiation and disease progression is accompanied by multiplication of mtDNA number and increased mtDNA content. mtDNA content corellates with the stage of the disease. mtDNA mutations faciliate cell proliferation and inhibit apoptosis by increasing the production of ractive oxygen species (ROS). Cells harbouring mutated mtDNA have increased proliferation rate, as increased ROS concentration may act as an endogenous growth factor.

Submucosal arytenoidectomy is one of many surgical techniques used in the treatment of the median bilateral vocal fold paralysis. The technique evolved from the large extralaryngeal operation to the endoscopic, intralaryngeal procedure. Gradually it excluded tracheostomy from the methods of treatment of dyspnoea caused by bilateral vocal fold paralysis.We present two patients with bilateral vocal fold paralysis with dyspnoea, caused by the neoplastic mass primarily localised in the left lung. In both cases the nonmicrocellular carcinoma was diagnosed. Both patients had the left recurrent laryngeal nerve palsy for more than 18 months and the right nerve palsy for 10-14 days before admission, with concomitant dyspnoea.Both patients were successfully extubated, 24 hours after the operation. The breathing improved significantly. None of the patients had to be reintubated or tracheotomized.The Authors conclude, that the arytenoidectomy with laterofixation should be the method of choice in the treatment of the bilateral vocal fold paralysis caused by the lung cancer. The method does not exclude the upper airway from the respiratory tract which is of special importance for the patients with the lung problems.

Study the epidemiological and clinical features of patients attending the emergency in the Clinic during 12 months to think whether the emergency is still needed as a one of method of curing. 4892 patients attended the emergency. Parameters analyzed were: age, sex, hour and day of arrival, place of living, initial signs, hospitalization and surgical services. The most frequent reasons for coming to the emergency were: ear disease (32.2%--middle ear otitis), nose disease (662 patients), bleeding nose (559 patients). The most frequent reason for hospitalization were swallowed foreign body (16.5%), tumor of the larynx and pharynx (16%), vestibulary nerve (12.9%). Emergency is an important sector of hospital activity, with a mean 55 per day (week-days), 87 per day (week-end and out of job days). The majority men disease were facial traumas, women were disease of vestibulary nerve, sudden hearing loss. However, 33% of the consultation in the emergency apper to be real medical emergencies, others could be appropriately provided by a general practitioner.

Several studies have shown that an opioid receptor antagonist, naltrexone, decreases palatable food consumption. Naltrexone has also been reported to reduce ethanol intake in alcohol-preferring rodents and human alcoholics. The aim of the present study was to assess the effects of naltrexone on taste and smell responses in healthy male volunteers. Naltrexone did not alter intensity and pleasantness of sucrose, quinine, citric acid, sodium chloride, and ethanol taste. Similarly, ratings of olfactory stimuli (orange extract and ethanol) and Coca-Cola flavor were not influenced by the opioid antagonist. Our findings may indicate that: (i) naltrexone exerts marginal, if any, effects on gustatory and olfactory responses in humans; (ii) the drug does not alter orosensory responses to ethanol.

Recent studies have indicated that glutamatergic NMDA receptors in the cochlea may be involved in ototoxic effects of aminoglycosides in animal subjects. Aminoglycoside antibiotics enhance the function of NMDA receptors by interaction with a polyamine modulatory site. Accordingly, high doses of aminoglycosides may increase calcium entry through the NMDA receptor-associated channel and promote degeneration of hair cells and cochlear nerve fibers. In line with the above, a polyamine site antagonist, ifenprodil as well as a high-affinity channel blocker, dizocilpine (MK-801) attenuates ototoxic effects of aminoglycosides in rats. Notably, ifenprodil as well as low-affinity channel blockers (e.g. memantine and amantadine) may be safely used in humans. Taken together, the above findings seem to open new avenues of research on selective pharmacotherapy of aminoglycosides-induced ototoxicity in humans.